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WHAT IS AN EKG? ~ Gutman 2012
(References Mosby,Bates,AHA,eMedicine Google Images,NAEMSE,NAEMT,
3 main vessels feed the heart: RCA, LAD, LCX. Their
distribution in each invidual is different but generally
 Right coronary artery (RCA) perfuses right side (or
bottom) of the heart in the Inferior territory (right
ventricle). Has a branch called the posterior descending
(PD) that feeds the back of the heart (posterior)
Left main divides into the left anterior descending
(LAD) (anterior LV territory) & the circumflex (LCX)
(lateral LV territory). Left main is the “Widowmaker” as a blockage here threatens the LAD & LCX.
The same kind of thing can happen on the right side: a
single occlusion can threaten the inferior territory (RCA),
and the posterior one (PDA, or just PD in this diagram:
“Posterior descending artery”, which perfuses the back of
the heart. Infero-posterior.
The heart lies on its side in the chest, with the RV
downwards, inferiorly. This territory is perfused by the right
coronary artery. The inferior part of the heart is innervated
partly by the same structures that innervate the stomach –
the wall of the one organ lying near the other which is why
people with inferior ischemia or infarct often have nausea
or vomiting, or sometimes hiccups in place of anginal pain ~ an “anginal equivalent”. An infarct here is an
inferior MI. A person with ischemia in the RCA is having “inferior ischemia”, which does not mean that it’s
less important than any other kind!
A 12 lead EKG primarily looks at the anterior part of the heart, the septal and anterior parts of the left
ventricle, which are (mostly) perfused by the left anterior descending artery. It makes sense that V1 and
V2 would be right over the cardiac septum?
And, this being the left side (says so, right there!),
Anterior LV (LAD): V2 (septal overlap)
V3, V4.
All the way around (or in latin:
“circumflex”) is lateral LV territory, V5,
V6, (with leads I & AVL.) Infarcting the
LAD territory produces an anterior MI.
V5 and V6 are around the left side of the chest. Along with I and AVL, they reflect the lateral part of the
left ventricle - also Big Pump territory. This part of the heart is perfused by the circumflex artery.
Also remember that the recall that the left main artery divides into the LAD and the LCX, which between
them perfuse most of the left ventricle. Take another look at that diagram of the arteries – see how the
left main supplies the two Big Pump arteries? A left main artery occlusion will threaten both areas of the
LV at the same time, and will produce an antero-lateral MI, with characteristic EKG changes in V2-4, as
well as I,L, and/or V5-6.
Septal leads are right in the center of the chest, and look at the septum between the ventricles. The
septum is perfused partly by the RCA, and partly by the LAD. A septal MI would show in V1 and V2.
Take a moment a refresh your mind as to the normal
appearance of the EKG complex The electrical impulse
originates in SA Node
Rhythm ► Regular (R to R Interval)
Rate ► Regular (60 – 100 beats/minute)
P wave ► before every QRS complex
QRS ► narrow, not wide (0.04-0.10sec)
Ischemia and the stages of an MI are different processes and produce
different kinds of changes in the normal complex of an EKG. The normal
complex goes through a whole series of evolutions as theheart goes
through an MI But in ischemia, what you get is usually ST depression,
below the isoelectric line
Not depressed.
Way depressed.
Or you could see flipped T waves
Ischemic EKG with ST
depressions in II? III, and
AVF. Nice! So where in the
heart? Which territory?
Which artery? Is anything
else going on?
(answer - “rate-related
ischemia on all areas of
the heart at once)
Quick look at the whole process.
This way…
First Stage: Acute Injury (ST Elevations)
Take a look at the QRS complex. The arrow on the left is pointing at the R-wave, which rises from the
isoelectric line, the flat part after the QRS. If clot occludes the
lumen, the process of infarction begins. 3 stages in progression of
the MI – the first is ‘acute injury’ lasting approximately 6 hours and
represents the period of time between the acute blockage of the
lumen, and the start of tissue death in the part of the heart that is
distal to that plug. This is the time frame that TPA or cardiac
catherization must be done within to save the heart muscle. This
stage of infarct will show as ST elevation in all the leads that reflect
whichever part of the heart is being affected
See how the S-wave doesn’t go all the way back down, and holds
the T-wave up with it? S-T elevation. Early-stage, acute injury MI.
These are really elevated “Tombstones”…
2nd Stage: Necrosis (Q-waves)
Take a look at the QRS complex. Is there really a Q-wave
here? See that little tiny
wave there at the end of the PR interval - a “non-pathologic” qwave. Normally the first move that a QRS complex makes after
the PR interval is to go – which way? Who said “Up!”? Yes,
correct. Up is right. See that? Up, after the PR?
Big q-waves represent the progression of the MI from the stage of
acute injury to the stage of necrosis. They show up as the QRS
moving downwards first, after the PR interval.
Look at all the upward Qs on this EKG! Easy to “misdiagnose” as
just part of the QRS if you don’t look closely.
What about V1? Looks like a big q-wave: a downward movement after the PR. But see – is it the only one
there is? V1 goes with which other lead? (V2.) Is there a q-wave there as well? (No.)
Here’s another one. See the PR interval? What does this QRS do – go up first, or down
first? Down is correct. This is definitely a “pathologic” q-wave: greater than a third of
the total size of the QRS. This one is the whole size of the QRS!
The appearance of q-waves means that the patient has missed the time “window” for clot lysis – which
makes sense, considering that the artery has now been plugged for more than four to six hours. See the
ST elevations, and the Q’s, all at the same time? This person is evolving from the first stage to the second
– moving from the stage of acute injury to the stage of necrosis. The ST segments will come back down to
the baseline (the “isoelectric” line) as the Q’s develop.
ST elevations, sliding back downwards as the Q waves grow
3rd Stage: Resolution (Persistent Q’s, or flipped T’s):
The resolution stage represents the development of scar tissue in the infarcted area, roughly two weeks
after the necrotic stage of the MI. The affected part of the heart will still show EKG changes, possibly
forever – ‘persistent Q-waves’, or flipped T-waves. Unless he’s having ischemia again! So…to summarize:
Before the MI
1st Stage
Resolution: the Q’s remain, and maybe flipped T as well…
or not.
Some EKG lead “mirror each other” electrically, so that ST elevations in one group will show up as ST
depressions in the other. Not ischemia – “mirroring”. There are only two main areas of the heart that do
this: the inferior and lateral ones; the septal and posterior ones. A set of inferior ST elevations in II, III and
AVF can produce lateral ST depressions in I, AVL, V5 and V6. it’s a reflection, bouncing electrically across
the heart from the inferior injury, showing up in reverse. The trick is to remember that when assessing
EKG changes, ST elevations always come FIRST. If there are ST elevations anywhere on an EKG, you
should wonder if any ST depressions on the same EKG might be reciprocal, instead of ischemic.
Inferior MI, lateral reciprocity.
Identify the primary process of inferior ST elevations? Now - see the ST depressions in I, and AVL lateral
leads? That’s not ischemia – it’s the “mirrored reflection” of the inferior MI. See the ST depressions in V1
and V2? This is posterior reciprocity, it makes sense that it would show up in this situation (think back to
the blood vessel anatomy).
Lateral MI, inferior reciprocity.
See the subtle ST elevations, this time in I and AVL? The primary process is a lateral MI. What’s happening
in the inferior leads? Not ischemia.
Posterior reciprocity
The septal leads (front of the heart) reflect a posterior event (back of the heart) in the same way that the
inferior/lateral ones do, but it’s difficult, since reading the posterior leads is made sort of difficult by the
fact that there aren’t posterior leads on a normal 12 lead EKG. On an EKG, the way you look at the back of
the heart, is by looking at the leads that look at the front of the heart, only backwards and upside down.
Here are a couple of sets of septal leads: V1 and V2.
Now – here are the same groups of leads, flipped and reversed:
ST elevations!
See the ST elevations? This is what you would see if you put real posterior leads on the patient. Posterior
MI. MDs do just this with an EKG – they’ll flip it over and hold it up to the light, looking for just this effect.
Sometimes the clue is if the patient having an inferior MI - The RCA perfuses both the inferior and
posterior areas – is there ST elevation in II, III and AVF? And ST depression in V1 and V2? Those septal
leads are giving you a “mirror” of an infarct process, rather than showing ischemia: an infero-posterior MI.
Right-Ventricular MI
Posterior events associated with inferior ones, because the posterior heart perfused by the posterior
descending artery (PDA), which branches off the right coronary artery (RCA) affecting these two areas at
once. Both inferior & posterior territories affected by a single RCA plug, producing an infero-posterior MI.
Infarcting this territory produces a “right ventricular” MI/
RVMI. 50% of all inferior MIs affect enough RV territory to
“stun” them into “hypokinetic inactivity” – dead tissue doesn’t
pump. To see this on an EKG, you need to do a 12-lead with
the chest leads applied backwards – going around towards the
right, instead of towards the left.
RVMIs are a different than left-sided MIs consisting primarily
of pressure & fluid management issues. In a right-ventricular
MI, the ventricle becomes hypokinetic (“It doesn’t move
much.”) instead of sending pumping effectively.
If the blood doesn’t get pumped to the lungs, how is it going to
get through those lungs and over to the other side, so blood
can get pumped out into the arteries, which is how you create a blood pressure? The LV needs a steady
supply to work with – rather than being and overloaded, it suddenly doesn’t have enough volume or
“preload” coming in.
These patients get liters of volume, to flood that sluggish RV and keep the blood moving - the opposite of
a left-system MI. Never give NTG – as this just drops the pressure (coronary artery vasodilator) and makes
your patient management more difficult and may cause cardiogenic shock that requires a balloon-pump.
Acute Injury - Stage 1
Look at the ST elevations in leads II, III and AVF in this first EKG. Important question: what kind of MI is
this? Which territory is being affected? Anterior? Inferior? Lateral? Septal? Is it too late for clot lysis, you
think, or is there still time (i.e are there Q waves)?
There is also some reciprocity: see the ST depressions in I and AVL? That would be lateral territory, which
is reciprocal to, or reflective of the Inferior territory. So what kind of MI is this? Which coronary artery is
being affected? What about the PDA?
Necrosis - Stage 2
How about now? Same kind of MI, same territory. But now things are looking a little different down there
in II, III and AVF. See how the Q-waves are starting to show up?
There is interesting reciprocity happening here: remember, ST elevations always come first in
interpretation. The inferior territory “reflects” the lateral one. So the ST elevations in the one show up as
ST depressions in the other. Sure enough: I is a little depressed, AVL is definitely depressed, but once
again I think V5 and V6 are sitting this one out.
How about the ST depressions in V1 and V2? Could be septal … I think this is yet another inferiorposterior MI. This person’s primary process is an IMI, right? The RCA perfuses the back of the heart so
the ST depressions are “mirrored” – they’re “reflecting” an ST elevation process going on, way in back
there. And what’s going on with V3 and V4?
Resolution - Stage 3
What rhythm is this? In this “post-MI” EKG, find the “persistent” Q-waves in II, III, and AVF. See the
evolution of an inferior MI from the acute stage, to necrosis, to resolution?
What’s Going On in this EKG?
Systematically: Lead I shows ST elevation = MI. Lead I goes with AVL, V5 and V6: ST elevations throughout
the lateral territory – possibly a circumflex infarct. After starting with lead I, go on to lead II: anything
there? Small QRS…how about the rest of the group: III and AVF? ST depressions in III for sure, maybe just
a little in AVF. So - lateral ST elevation, inferior ST depression… remember that ST elevations always come
first in interpretation? So ST elevations laterally…and infarct is always interpreted as the main process…
Inferior reciprocity! Check the chest leads: V1 q-wave! V2, V3, V4 – big anterior ST elevations already
starting to form q’s…another infarct area! So there are two areas with ST elevations: the lateral group,
and the anterior group. That would mean infarct in the circumflex and the LAD…in other words - a left
main lesion!
Normal Sinus Rhythm
Rhythm – Regular; Rate - 60-100 bpm; QRS Duration – Normal; P Wave - Visible before each QRS complex
P-R Interval - Normal (<5 small Squares. Anything above and this would be 1st degree block)
Sinus Bradycardia
Heart rate <60 bpm. can be normal, but may be due to increased vagal tone; Rhythm – Regular; Rate - <60
bpm; QRS Duration – Normal; P Wave - Visible before each QRS complex; P-R Interval – Normal
Sinus Tachycardia
Heart rate >100 bpm, originates in SA node. Causes include stress, fright, illness, exercise. Impulse
generating heart beats is normal, but occurring at a faster pace than normal.
Rhythm – Regular; Rate - > 100 bpm; QRS Duration – Normal; P Wave - Visible before each QRS complex;
P-R Interval – Normal
Supraventricular Tachycardia (SVT)
Narrow complex atrial tachycardia not controlled from SA node, instead coming from a collection of tissue
around the atrioventricular (AV) node
Rhythm – Regular; Rate - 140-220 beats per minute; QRS Duration - Usually normal; P Wave - Often
buried in preceding T wave; P-R Interval - Depends on site of supraventricular pacemaker
Atrial Fibrillation
Many atria foci generating own electrical impulses, leading to irregular impulse conduction to ventricles.
Rhythm - Irregularly irregular
Rate - 100-160 BPM but slower if on medication; QRS Duration - Usually normal; P Wave - Not
distinguishable as the atria are firing off all over; P-R Interval - Not measurable
Atrial Flutter
Abnormal tissue generating rapid atrial heart rate, however AV node not involved.
Rhythm – Regular; Rate – Usually 150 bpm; QRS Duration - Usually normal; P Wave - Replaced with
multiple F (flutter) waves, usually at a ratio of 2:1 (2F - 1QRS) but sometimes 3:1; P Wave rate - 300 bpm;
P-R Interval - Not measurable
1st Degree AV Block
Conduction delay through AV node but all electrical signals reach the ventricles. Generally benign.
Rhythm –Regular; Rate – Normal; QRS Duration – Normal; P Wave - Ratio 1:1; P Wave rate – Normal;P-R
Interval - Prolonged
2nd Degree Block Type 1 (Wenckebach)
Conduction block of some but not all atrial beats getting through to the ventricles. Progressive
lengthening of PR interval then failure of conduction of atrial beat with dropped QRS complex.
Rhythm - Regularly irregular; Rate - Normal or Slow; QRS Duration – Normal; P Wave - Ratio 1:1 for 2,3 or
4 cycles then 1:0.; P Wave rate - Normal but faster than QRS rate; P-R Interval - Progressive lengthening of
P-R interval until a QRS complex is dropped
2nd Degree Block Type 2
Electrical excitation intermittently fails to pass through AV node or bundle of His.
Rhythm – Regular; Rate - Normal or Slow; QRS Duration – Prolonged; P Wave - Ratio 2:1, 3:1
P Wave rate - Normal but faster than QRS rate; P-R Interval - Normal or prolonged but constant
3rd Degree Block
Atrial contractions normal but no electrical conduction to ventricles. Ventricles generate own slow signal
through an escape focus within the ventricle.
Rhythm – Regular; Rate – Slow; QRS Duration – Prolonged; P Wave – Unrelated; P Wave rate - Normal but
faster than QRS rate; P-R Interval - Variation
Bundle Branch Block
Abnormal conduction through bundle branches causes a depolarization delay through ventricles.
Rhythm – Regular; Rate – Normal; QRS Duration – Prolonged; P Wave - Ratio 1:1; P Wave rate - Normal
and same as QRS rate; P-R Interval - Normal
Premature Ventricular Complexes
Ventricles depolarize prematurely in response to a signal within the ventricles.
Rhythm – Regular; Rate – Normal; QRS Duration – Normal; P Wave - Ratio 1:1; P Wave rate - Normal and
same as QRS rate; P-R Interval – Normal
Junctional Rhythms
Impulse generated below the atria.
Rhythm – Regular; Rate - 40-60 Beats per minute; QRS Duration – Normal; P Wave - Ratio 1:1 if visible.
Inverted in lead II; P Wave rate - Same as QRS rate; P-R Interval - Variable
Ventricular Tachycardia (VT)
Results from abnormal tissues in ventricles generating rapid and irregular heart rhythm.
Rate – 150-250 Beats per minute; QRS Duration – Prolonged; P Wave - Not seen
Ventricular Fibrillation (VF)
Disorganized electrical signals cause ventricles to quiver instead of contract in a rhythmic fashion. A
patient will be unconscious as blood is not pumped to the brain.
Rhythm – Irregular; Rate - 300+, disorganized; QRS Duration - Not recognizable; P Wave - Not seen
Rhythm – Flat; Rate - 0 Beats per minute; QRS Duration – None; P Wave - None

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